Alpha-tocopherol consumption during low-density-lipoprotein oxidation.
1. The kinetics of the depletion of alpha-tocopherol in human low-density lipoprotein (LDL) were measured during macrophage-mediated and cell-free oxidation. The formation of oxidatively modified, high-uptake species of LDL in these systems was not detectable until all of the endogenous alpha-tocopherol had been consumed. 2. Supplementation of the alpha-tocopherol content of LDL by loading in vivo extended the duration of the lag period during which no detectable oxidative modification occurred. 3. The addition of a flavonoid (morin) prevented both alpha-tocopherol consumption and oxidative modification of LDL. 4. The alpha-tocopherol contents of LDLs from a range of individual donors could not be used to predict their relative resistance to oxidation, indicating that other endogenous antioxidants may also be present, and quantitatively significant, in human LDL.
Jessup
W
W
Department of Biology and Biochemistry, Middlesex, U.K.
Rankin
S M
SM
De Whalley
C V
CV
Hoult
J R
JR
Scott
J
J
Leake
D S
DS
D000818:Animals; D002478:Cells, Cultured; D003300:Copper / Q000494:pharmacology; D019327:Copper Sulfate; D004032:Diet; D005260:Female; D006801:Humans; D007700:Kinetics; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D010084:Oxidation-Reduction; D014810:Vitamin E / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology
D008077:Lipoproteins, LDL; D014810:Vitamin E; D003300:Copper; D019327:Copper Sulfate